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Special Report From the National Institute of Neurological Disorders and Stroke Classification of Cerebrovascular Diseases III Contents

Introduction Outline I. Clinical Disorders II. Pathology (outline format only) Background Material HI. Risk Factors and Prevention IV. Clinical Assessment V. Evaluation A. Laboratory B. Neurophysiologic C. Cardiovascular D. Brain Imaging E. Vascular 1. Noninvasive 2. Invasive—Angiography F. Cerebral Blood Flow and Metabolism VI. Status of Patient Following Stroke VII. Anatomy (outline format only) Classification I. Clinical Disorders II. Pathology (see outline) Background Material III. Risk Factors and Prevention IV. Clinical Assessment V. Evaluation A. Laboratory B. Neurophysiologic C. Cardiovascular D. Brain Imaging E. Vascular 1. Noninvasive 2. Invasive—Angiography F. Cerebral Blood Flow and Metabolism VI. Status of Patient Following Stroke VII. Anatomy (see outline)

A report by a committee established by the Director of the National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland. Committee: Jack P. Whisnant, MD, chairman; Jeffrey R. Basford, MD; Eugene F. Bernstein, MD; Edward S. Cooper, MD; Mark L. Dyken, MD; J. Donald Easton, MD; John R. Little, MD; John R. Marler, MD; Clark H. Millikan, MD; Carol K. Petito,

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MD; Thomas R. Price, MD; Marcus E. Raichle, MD; James T. Robertson, MD; Brian Thiele, MD; Michael D. Walker, MD; and Robert A. Zimmerman, MD. Address for reprints: Division of Stroke and Trauma, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Received November 21, 1989; accepted November 30, 1989.

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Introduction The purpose of this Classification of Cerebrovascular Diseases III is to delineate the types of cerebrovascular disease in clinical and pathological terminology so that all or any portion of the classification may be used by clinicians, surgeons, pathologists, or physiatrists as well as by other groups interested in the subject. It is also intended to define clinical and pathological diagnostic terms for common use. The background material is intended as supporting information for the clinical and pathological classifications. The second Ad Hoc Committee on Cerebrovascular Diseases1 developed a classification, published in 1975, that provided a clinical and pathological framework for cerebrovascular diseases at that time. The Classification and Outline of Cerebrovascular Diseases II was published near the beginning of an explosion in technological developments that have dramatically enhanced our capability to evaluate patients with these disorders. Technological advances will continue, but the present Classification of Cerebrovascular Diseases III and background material reflect the current state of our knowledge. By the term "cerebrovascular diseases" we refer to all disorders in which there is an area of brain transiently or permanently affected by ischemia or bleeding and/or in which one or more blood vessels of the brain are primarily impaired by a pathological process. The terms "cerebrovascular" and "cerebral" are used in the original Latin sense, referring to the

entire brain and not merely to the hemispheres of the forebrain. The term "stroke" is commonly used as a generic term to represent any one or all of a group of disorders, including cerebral infarction, intracerebral hemorrhage, or subarachnoid hemorrhage. The background material supporting the Classification of Cerebrovascular Diseases III recognizes the potential impact of preventive measures on stroke occurrence. It also recognizes the enhancements of our capabilities .o define anatomic lesions in the brain and in the blood vessels in living patients by technological developments. The outline summarizes the classification of the clinical and pathologic disorders and the background material on prevention, clinical assessment, evaluation, status of the patient following stroke, and anatomy. The anatomy and pathology are sufficiently defined in the outline; therefore, the descriptive material, which follows the outline precisely, does not provide information for anatomy and pathology. The document begins with the classification and then provides an orderly format for proceeding from prevention through clinical assessment and evaluation to the poststroke status of the patient and to the organization of the anatomical terms. It is intended that the classification, or the supporting material, should be useful to the various disciplines that are concerned with clinical service, training, or research in the cerebrovascular diseases.

Outline Clinical Disorders A. Asymptomatic B. Focal Brain Dysfunction 1. Transient Ischemic Attacks (TIAs) a. Carotid system b. Vertebrobasilar system c. Both d. Uncertain location e. Possible TIA 2. Stroke a. Temporal profile 1) Improving 2) Worsening 3) Stable stroke b. Types of stroke (for details see II. Pathology) 1) Brain hemorrhage 2) Subarachnoid hemorrhage (SAH) 3) Intracranial hemorrhage from arteriovenous malformation (AVM) 4) Brain infarction a) Mechanisms (1) Thrombotic (2) Embolic (3) Hemodynamic

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b) Clinical categories (1) Atherothrombotic (2) Cardioembolic (3) Lacunar (4) Other (see II. Pathology) c) Symptoms and signs by site (distribution) (1) Internal carotid artery (2) Middle cerebral artery (3) Anterior cerebral artery (4) Vertebrobasilar system (a) Vertebral artery (b) Basilar artery (c) Posterior cerebral artery C. Vascular Dementia D. Hypertensive Encephalopathy II.

Pathology A. Pathologic Alterations in Heart and Blood Vessels 1. Arteries (and arterioles, when applicable) a. Congenital, developmental, and inherited lesions 1) Aplasia of artery 2) Hypoplasia of artery 3) Anomaly of artery (fetal form) 4) Redundancy (loops), dilatation, or elongation of artery 5) Genetically determined defects in arteries a) Marfan's syndrome (arachnodactyly) b) EhJers-Danlos syndrome c) Pseudoxanthoma elasticum d) Others 6) Vascular malformations a) AVM b) Cavernous hemangioma c) Capillary telangiectasia b. Saccular aneurysm 1) Unruptured 2) Ruptured c. Atherosclerosis 1) Stenosis 2) Occlusion 3) Ulceration of plaque 4) Hemorrhage in plaque 5) Dilatation, ectasia, fusiform aneurysm d. Hypertensive alterations 1) Arteriolar sclerosis 2) Hyaline medial degeneration with or without fibrinoid change 3) Charcot-Bouchard microaneurysm 4) Other e. Arterial embolism—Sources 1) Heart a) Cardiac valvular disease (including mitral and aortic valve disease, prosthetic valve, mitral valve prolapse) (1) Septic (2) Nonbacterial thrombotic endocarditis (3) Libman-Sacks endocarditis (4) Other b) Cardiac atrium (including atrial fibrillation, myxoma, aneurysm) c) Cardiac ventricle (including myocardial infarction, aneurysm, dyskinesia of wall, ventricular assist device) 2) Aorta and major branches a) Ulcerative plaque

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Plaque plus thrombus Fibromuscular dysplasia Spontaneous arterial dissection 3) Paradoxical embolus a) Venous thrombosis b) Other 4) Tumor 5) Trauma-related embolism a) Fat b) Bone marrow c) d)

Air

Arterial dissection Inflammatory arteritis 1) Infectious a) Etiology (1) Bacterial (2) Fungal (3) Viral (4) Rickettsial (5) Other b) Pathogenesis (1) Meningoencephalitis (2) Septic emboli (3) Other c) Complications (1) Thrombosis (2) Hemorrhage (3) Scar (4) Pseudoaneurysm 2) Noninfectious a) Etiology (1) Cranial (temporal) arteritis (2) Periarteritis nodosa (3) Other* b) Complications (1) Thrombosis (2) Hemorrhage (3) Scar (4) Pseudoaneurysm g- Toxic, metabolic, and systemic disorders 1) Thrombosis a) Dehydration b) Drugs (specify) c) Blood dyscrasias (specify type) d) Other 2) Hemorrhage a) Anticoagulants (specify) b) Thrombolytic drugs c) Sympathomimetic amines (including illicit drugs) d) Heavy metals e) Blood dyscrasias f) Other 3) Calcification or mineralization a) Hypoparathyroidism b) Hypervitaminosis D c) Monckeberg's sclerosis (calcific medial arteriosclerosis) d) Mineralization (ferrugination, calcification, siderocalcification) (1) Infection (specify) •Although common terminology employs the term "lupus vasculitis," a true inflammatory arteritis in the central nervous system in patients with systemic lupus erythematosus is exceedingly rare and therefore is not specifically indexed here.

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(2) Idiopathic (age-related) (3) Familial (4) Other h. Traumai or physical agents 1) Mechanisms a) External forces, bony anomalies, fractures, dislocations, degenerative bone disease, fibrosis b) Intra-arterial interventional procedures (1) Angiography (2) Cardiac catheterization (3) Balloon occlusion (4) Transluminal angioplasty (5) Pump oxygenation (6) Embolization (7) Drug therapy c) Surgery or interventional procedures (1) Reconstructive and reparative arterial surgery (2) Other surgical procedures (a) Occlusion (ligation, clamp, etc.) (b) Rupture or accidental division d) Brain herniation (transtentorial, subfalcial, foramen magnum, etc.) e) Radiation (1) Acute (2) Delayed 2) Pathologic consequences a) Vasospasm b) Compression c) Intramural hemorrhage (1) With dissection d) Rupture of atherosclerotic plaque (1) With atheromatous embolization e) Necrosis f) Thrombosis g) Fibrosis, hyalinization h) Stenosis i) Accelerated atherosclerosis j) Embolization due to foreign materials k) Pseudoaneurysm Neoplastic disease 1) Thrombosis a) Intracranial neoplasm (primary or secondary) b) Extracranial neoplasm c) Intravascular neoplasm 2) Hemorrhage a) Intracranial neoplasm (primary or secondary) b) Extracranial neoplasm 3) Embolism a) Intracranial neoplasm (primary or secondary) b) Extracranial neoplasm 4) Intravascular malignant lymphomatosis (malignant angioendotheliosis) Amyloid (congophilic) angiopathy 1) Location a) Meningeal b) Parenchymal 2) Secondary effects a) Hemorrhage b) Focal atrophy (scar) c) Infarct 3) Associated factors a) Familial

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Stroke Vol 21, No 4, April 1990 b) Senile dementia of Alzheimer's type c) Other k. Miscellaneous disorders of arteries 1) Fibromuscular dysplasia 2) Thromboangiitis obliterans 3) Hemorrhagic dissection of arterial wall 4) Other 2. Veins (and venules, when applicable) and Venous Sinuses a. Congenital, developmental, and inherited lesions 1) Anomaly of veins (fetal form) 2) Anomaly of veins (unspecified) 3) Aneurysm of veins, congenital (phlebectasia) a) Ruptured aneurysm, congenital 4) Malformation a) AVM b) Dural AVM c) Venous angioma (varix) b. Inflammatory lesions of veins 1) Infectious a) Etiology (1) Bacterial (2) Fungal (3) Viral (4) Other b) Pathogenesis (1) Meningoencephalitis (2) Trauma (3) Other c) Complications (1) Thrombosis (2) Hemorrhage 2) Noninfectious a) Venous lesions due to toxic, metabolic, or systemic disorders (1) Thrombosis (a) Dehydration (b) Drugs (specify) (c) Blood dyscrasias (specify type) (d) Other (2) Hemorrhage (a) Anticoagulants (b) Heavy metals (c) Blood dyscrasias (d) Other c. Trauma 1) Mechanisms a) Surgery involving veins (1) Embolization (specify) (2) Thrombosis (3) Thrombosis in venous anastomosis or grafts b) Other surgical procedures (1) Occlusion (ligation, clamp, etc.) (2) Rupture or accidental division (3) Intramural hemorrhage (4) Thrombosis (a) With embolization c) Brain herniation (subfalcial, foramen magnum, etc.) (1) Thrombosis (2) Hemorrhage d) Radiation (1) Postirradiation thrombosis (2) Postirradiation scar (fibrosis)

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2) Pathologic consequences a) Compression b) Hemorrhage c) Thrombosis d. Calcification or mineralization 1) Hypoparathyroidism 2) Hypervitaminosis D 3) Infection 4) Other e. Associated with neoplastic disease 1) Thrombosis a) Intracranial neoplasm (primary or secondary) b) Extracranial neoplasm 2) Hemorrhage a) Intracranial neoplasm (primary or secondary) b) ExtracTanial neoplasm 3) Embolism a) Intracranial neoplasm (primary or secondary) b) Extracranial neoplasm f. Other 3. Capillaries a. Petechiae associated with inflammation 1) Infectious 2) Noninfectious b. Petechiae due to trauma and physical agents 1) External trauma 2) Remote effects of trauma a) Fat embolization b) Bone marrow embolization c) Air embolization 3) Angiography 4) Therapeutic intravascular procedures 5) Surgery 6) Brain herniation 7) Heat stroke 8) Radiation c. Capillary lesions associated with toxic, metabolic, or systemic disorders 1) Petechiae a) Anticoagulants b) Drugs c) Heavy metals or toxins (specify) d) Metabolic disturbances e) Blood dyscrasias (including thrombocytopenia, disseminated intravascular coagulation, and thrombotic thrombocytopenic purpura) f) Other 2) Thrombosis a) Dehydration b) Drugs c) Blood dyscrasias (see above) d) Other 3) Calcification or mineralization a) Hypoparathyroidism b) Hypervitaminosis D c) Infection d) Other d. Miscellaneous capillary lesions e. Other B. Pathologic Alterations in Brain and Spinal Cord 1. Infarct* •Subcortical cystic infarcts 24 hours but clear up in 1-3 weeks (sometimes referred to as a reversible ischemic neurologic deficit [RIND]). b. Types of stroke Determination of stroke type can be crucial to rational treatment and prediction of outcome. With the use of CT and MRI and lumbar puncture, bleeding into and around the brain can be diagnosed and these types of stroke separated from the more common infarction. Subtypes of infarction can be diagnosed or suspected on the basis of the presence of other disease, the presentation and findings on examination, and the findings on brain imaging. 1) Brain hemorrhage Approximately 10% of all strokes are due to brain hemorrhage. Hypertension, especially uncontrolled hypertension, is the leading condition associated with brain hemorrhage. Other predisposing conditions include ruptured aneurysm; AVM; cavernous angioma; drug abuse with cocaine, amphetamines, or alcohol; blood dyscrasia; anticoagulant therapy; amyloid angiopathy; and brain tumor. The clinical features of brain hemorrhage vary depending on the location and severity of the bleeding. It is unlikely to be preceded by TIAs. The process is usually acute, frequently with severe headache and a decreased level of consciousness. Usually, the blood pressure is elevated at the time of the initial examination, even if there was no preexisting hypertension. (The clinical state can be graded according to the level of consciousness.) The most common locations of hypertensive bleeding are the basal ganglia, thalamus, lobe of a hemisphere, cerebellum, or pons. Deep hemispheric hemorrhages typically produce a contralateral hemiparesis and hemisensory deficit with aphasia in those patients with the dominant hemisphere involved. Aphasia can occur in cases of hemorrhage into the thalamus of the dominant hemisphere. The presence of oculomotor findings such as forced downgaze or upgaze palsy, unreactive miotic pupils, and convergence paralysis are characteristic of thalamic hemorrhage and help to differentiate it from putaminal hemorrhage. Patients with lobar hemorrhage into the cortex or subcortical white matter less frequently have a history of hypertension than those with deep hemorrhage. In elderly persons, amyloid angiopathy is a common cause of lobar hemorrhage. Headache is a common feature. Disturbance of the level of consciousness also occurs less often and is seen later in the clinical course. The neurologic deficits are more variable than in deep hemorrhage and depend upon the location and size of the hematoma. Cerebellar hemorrhage usually occurs in one of the hemispheres, originating in the region of the dentate nucleus. Disequilibrium, limb ataxia, nausea, and vomiting are

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common early features. Patients with cerebellar hemorrhage frequently complain of headache and dizziness. The examination usually demonstrates a combination of signs indicative of cerebellar and pontine dysfunction. Peripheral facial palsy, nystagmus, miosis, decreased corneal reflex, and abducens palsy are the most common brainstem and cranial nerve findings. Primary hemorrhage into the brainstem usually has devastating effects, but occasionally a small hemorrhage occurs, producing limited dysfunction compatible with functional survival. The neurologic deficit resulting from hemorrhage depends on the level of brainstem involvement, with the pons being the most common site. Symptoms and signs may not distinguish brain hemorrhage from other stroke types, even though many patients with brain hemorrhage have untreated hypertension, and a large proportion present with obtundation and focal deficit. CT reliably shows intraparenchymal hemorrhage. Since the widespread use of CT, it has become evident that a number of patients with a small brain hemorrhage will present with little headache or obtundation and a deficit indistinguishable from that of infarction. Thus, the only way to reliably diagnose hemorrhage is with the routine use of CT. A small percentage of patients with ischemic infarction will present with severe headache, rapid obtundation, and other clinical features indistinguishable from those of brain hemorrhage. Patients with brain hemorrhage rarely show any improvement in neurologic deficit during the first 24 hours. 2) SAH The characteristic clinical picture of primary SAH (in which the initial bleeding Js into the subarachnoid space) begins with the sudden onset of a severe headache. The suddenness of the onset and the severity of the pain are usually dramatic. The headache commonly reaches a severe intensity in a matter of seconds to a minute and is so severe as to alter the patient's pattern of activity. Often there is a rapid alteration of level of consciousness (including unconsciousness with recovery in a few minutes). Vomiting at onset is frequent. Patients with SAH may be younger and less likely to have hypertension and other underlying disease before the onset of the stroke than patients with other types of stroke. TABLE 1. Status (Grade) of Patients With Intracranial Aneurysm With and Without Subarachnoid Hemorrhage2

Grade 0 1 la 2 3 4 5

Symptoms and signs Unruptured aneurysm —no history or other manifestation of subarachnoid hemorrhage Asymptomatic or minimal headache and slight nuchal rigidity No acute meningeal or brain reaction, but fixed neurologic deficit Moderate to severe headache, nuchal rigidity, no neurologic deficit other than cranial nerve palsy Drowsiness, confusion, or mild focal neurologic deficit Stupor, moderate to severe hemiparesis; may also include early decerebrate rigidity and vegetative disturbances Deep coma, decerebrate rigidity,_moribund_appearance

The clinical grade (Table 1) at the time of initial evaluation is a good index of short-term prognosis. There are usually no focal findings on examination, but the likeliest single finding is a partial oculomotor nerve palsy. Most patients have a stiff neck on bending the head forward or other signs of meningeal irritation (Kernig's or Brudzinski's signs). Subhyaloid (preretinal) hemorrhage may be found on funduscopic examination. CT almost always shows blood in the subarachnoid space on the day of the hemorrhage, but there is a diminishing chance of finding blood with each day after the onset. In patients suspected of SAH who have a CT scan that does not show blood, lumbar puncture should be done to confirm the diagnosis. In SAH, the CSF will be bloody, and the supernatant will be xanthochromic within a few hours after the hemorrhage. SAH is usually due to a ruptured saccular aneurysm. The aneurysm can sometimes be viewed on CT or MRI, but usually an arteriogram demonstrating all the intracranial Downloaded from http://stroke.ahajournals.org/ by guest on June 13, 2016

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vessels is necessary to demonstrate the lesion. Vasospasm and infarction in the arterial distribution of the vasospasm are common causes of disability after the first 48 hours following the onset of SAH. Other causes of nontraumatic SAH include AVMs and neoplasms. In 10-15% of patients, no source can be demonstrated on complete angiography, and the prognosis is generally more favorable in such patients. 3) Intracranial hemorrhage from an AVM SAH, intracerebral hemorrhage, or a combination of both may occur from AVMs. It is characteristic that the hemorrhage has less pronounced symptoms and may be less severe than with ruptured aneurysms. There may be a history of seizures and sometimes focal cerebral symptoms and signs. In some patients, a bruit over the head may be present; in others, preretinal hemorrhage or retinal angiomas are present. 4) Brain infarction Patients with infarction generally have a medical history that includes one or more risk factors for stroke. That is, patients are unlikely to have been completely healthy before the stroke. Although many of the patients have hypertension, diabetes, and heart disease, previous TIAs and strokes are also common. Severe headache and vomiting are unusual at the onset of brain infarction. The deficit generally comes on rapidly and may continue to worsen over hours or days. Patients present with focal neurologic symptoms and signs, for example, hemiparesis and sensory impairment, with carotid-distribution infarctions. a) Mechanisms of ischemic infarction (1) Thrombotic Thrombotic infarction usually occurs when a thrombus is superimposed on an atherosclerotic plaque. In some circumstances thrombotic infarction may be precipitated by an abnormality of blood clotting. (2) Embolic Embolic infarction is due to occlusion of an artery by an embolus distal to a point where adequate collateral blood flow is available. (3) Hemodynamic Hemodynamically determined infarction most commonly occurs when there is severe stenosis or occlusion of the proximal arterial supply to a portion of the brain and collateral compensatory blood flow is inadequate while global cerebral perfusion is critically decreased (for example, with decreased cardiac output). b) Clinical categories Infarction is commonly considered to be atherothrombotic, cardioembolic, or lacunar. Perhaps 30-40% of patients with infarction cannot easily be classified clinically as having one of these types and are best labeled as having infarction of unknown type. Even if the usual differentiating criteria are met, the assumed diagnosis is not certain. (1) Atherothrombotic This type of infarction occurs with atherosclerosis involving selected sites in the extracranial and major intracranial arteries. There are two main ways in which atherosclerosis produces infarction. First, the plaque may enlarge to seriously compromise the lumen of a blood vessel, but more often this happens with a superimposed thrombus. When a vessel occludes, a stagnation clot may form above the original occlusion and propagate distally. The second mechanism by which an atherosclerotic plaque causes infarction is embolism of thrombus or plaque fragments (artery-to-artery embolus). A history of TIAs and cervical bruit is more frequently found in persons with atherothrombotic infarction than in those with other types of stroke. Clinical diagnosis rests on finding evidence of arterial stenosis or occlusion thought to be due to atherosclerosis at one or more sites. The infarct may be small and indistinguishable from a cardiac embolic infarct.

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(2)

Cardioembolic Although many authors have commented on the exceptionally rapid onset of this type of stroke, such is not uniformly the case. The onset begins with a focal deficit and worsening may occur. The basis for the clinical diagnosis is the demonstration of a cardiac-transcardiac source of embolus and no evidence of other causes of stroke. Cardiac conditions that may produce emboli include intermittent or continuous atrial fibrillation or flutter, recent myocardial infarction, congestive heart failure, and mitral or aortic valve disease. When the source is transcardiac by way of a right-to-left cardiac shunt (paradoxical embolus), the source of the clot is usually a peripheral venous thrombus. The diagnosis of cardioembolic infarction may be suggested by evidence of multiple brain or systemic infarcts. Ginical presentations that are often due to cardioembolism include isolated homonymous hemianopsia and isolated aphasia. By brain imaging, it is sometimes possible to see an infarct with some hemorrhage in it. Most cardioembolic infarcts involve the cortex and are commonly in the distribution of branches of the middle cerebral artery.

(3) Lacunar Although this is a pathological term, it is commonly used as a clinical category for the small lesions that result from involvement of deep, small, penetrating arteries. These arteries tend to branch at 90° from the main intracerebral arteries and supply the deep white and gray matter of the cerebral hemispheres (e.g., lenticulostriate arteries) and the brainstem. Since the arteries have poor collateral connections, obstruction of blood flow by arterial disease, thrombus, or embolus leads to infarction in the limited distribution of one of these arteries. Over time, the infarct becomes cystic and filled with fluid surrounded by normal tissue, hence the name "lacune" or lake. Clinical diagnosis usually rests on brain imaging or the clinical syndrome indicating the anatomic location. Brain imaging shows a small lesion (

Special report from the National Institute of Neurological Disorders and Stroke. Classification of cerebrovascular diseases III.

637 Special Report From the National Institute of Neurological Disorders and Stroke Classification of Cerebrovascular Diseases III Contents Introduc...
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